Biomedical subjects
H C Lin
Publications and source records attributed to H C Lin.
Portal hypotensive effects of tetrandrine and verapamil in portal hypertensive rats.
The portal hypotensive effects of tetrandrine and verapamil (both calcium-channel blockers) were assessed in portal hypertensive rats. Portal hypertension was induced by partial portal vein ligation in Sprague-Dawley rats. Both tetrandrine (4, 8, 16 and 24 mg kg-1) and verapamil (0.5, 1.0, 1.5 and 2.0 mg kg-1) induced dose-dependent decreases of portal venous pressure and mean arterial pressure after intravenous infusion. for example, infusion of tetrandrine (16 mg kg-1) induced a maximum reduction of portal venous pressure and mean arterial pressure approximately 1 min after the start of infusion. Portal venous pressure decreased from baseline (12.5 mmHg) to 10.0 mmHg, and mean arterial pressure from baseline (90 mmHg) to 80 mmHg. Heart rate decreased from 250 to 240 beats min-1. At 24 mg kg-1, tetrandrine reduced portal venous pressure and mean arterial pressure to 20.3 +/- 2.4% and 28.4 +/- 1.4% of baseline, respectively. Our results show that both tetrandrine and verapamil induce portal pressure reduction in portal hypertensive animals.
The hemodynamic effects of AT-112, an analog of ketanserin, in portal hypertensive rats.
A serotonin mechanism has been reported to contribute to the hyperdynamic circulation of portal hypertension. Different studies have demonstrated that serotonin antagonists decrease portal pressure in portal hypertensive patients and animals. The present study was undertaken to investigate the effect of AT-112, an analog of ketanserin, on portal hypertension induced by partial portal vein ligation in rats. Since ketanserin is known to possess alpha 1-adrenergic antagonistic activity, the effect of AT-112 was compared to that of prazosin. A single dose (prazosin 4.2 micrograms/kg, AT-112 1 mg/kg) was chosen to produce a similar hypotensive effect (-20 +/- 4% for prazosin and -24 +/- 4% for AT-112). At this dose, prazosin significantly decreased total peripheral resistance whereas AT-112 significantly decreased cardiac index and heart rate. Both agents significantly decreased the portal tributary blood flow and portal pressure. In rats receiving AT-112, a significant correlation was found between the magnitudes of decrease in cardiac index and the decrease in portal tributary blood flow. We also found that the magnitude of reduction in portal pressure was greater following AT-112 administration. This study suggested that AT-112 may have more beneficial hemodynamic effects than prazosin in portal hypertensive rats. Our results provide further support for the serotonergic mechanism in the pathogenesis of hyperdynamic circulation in portal hypertension.
Hemodynamic effects of chronic tetrandrine and propranolol administration on portal hypertensive rats.
The purpose of this study was to investigate the therapeutic effects of tetrandrine and propranolol, alone or in combination, on portal hypertensive rats. Portal hypertension was induced by partial portal vein ligation in Sprague-Dawley rats. Animals were allocated into one of the four groups: vehicle group (0.1 N.HCl, 0.7 ml/day), tetrandrine group (50 mg/kg/ day), propranolol group (30 mg/kg/day), and tetrandrine (50 mg/kg/day) plus propranolol (30 mg/kg/day) group. Drug or vehicle was administered by gavage for consecutive 9 days. After 9 days of treatment, the portal venous pressure and mean arterial pressure in each treatment group were significantly lower than those in the vehicle group. The cardiac index was not changed by tetrandrine alone, but reduced in the two groups receiving propranolol alone or in combination. Total peripheral resistance was significantly decreased in the tetrandrine group and significantly increased in the tetrandrine plus propranolol group as compared with the vehicle group. Our results suggested that tetrandrine or propranolol alone induced portal hypotensive effects, with propranolol achieving better antihyperdynamic effects in terms of cardiac index, and in combination propranolol effects predominated over those of tetrandrine.
Cardiovascular effects of nitric oxide and N-methyl-D-aspartate receptors in the nucleus tractus solitarii of rats.
Nitric oxide (NO) is an endogenously synthesized effector molecule that acts as a neurotransmitter with novel properties in both the central and peripheral nervous systems. We previously reported that NO was involved in central cardiovascular regulation and modulated the baroreflex in the nucleus tractus solitarii (NTS) of rats. The aim of the present study was to determine whether NO and excitatory amino acids reciprocally release each other in the NTS. In normotensive Sprague-Dawley rats, intra-NTS microinjection of L-arginine (1 to 100 nmol/60 nL) produced a dose-dependent decrease in blood pressure and heart rate. Microinjection of excitatory amino acids L-glutamate and NMDA also produced depressor and bradycardic effects. These effects of L-glutamate or NMDA were blocked by prior administration of NO synthase inhibitor N(G)-methyl-L-arginine or N(G)-nitro-L-arginine methyl ester. Similarly, prior administration of N-methyl-D-aspartate (NMDA) receptor antagonist MK-801 and non-NMDA receptor antagonist 6,7-dinitroquinoxaline-2,3-dione significantly attenuated the depressor and bradycardic effect of L-arginine. These results demonstrated a reciprocal attenuation of NO synthase inhibitor and NMDA receptor antagonist on NMDA and L-arginine responses, respectively, in the NTS and suggest that NO and NMDA receptors may interact in central cardiovascular regulation.
Inhaled gentamicin reduces airway neutrophil activity and mucus secretion in bronchiectasis.
To investigate whether aerosolized gentamicin (GM) prevents myeloperoxidase (MPO)-mediated airway injury and mucus hypersecretion, a short course of aerosol therapy (3 d) with GM 40 mg or 0.45% saline (saline) twice per day was conducted. Twenty-eight patients with bronchiectasis and mucus hypersecretion after adequate chest care and hydration were enrolled in a randomized, double-blind fashion. MPO levels in sputum collected on arising were determined by fluorometric assay at 655 nm before and after treatment. The sputum MPO level significantly decreased in patients receiving aerosolized GM, from 0.22 +/- 0.04 to 0.14 +/- 0.04 U/g (n = 15), but not in patients with saline inhalation (0.23 +/- 0.03 to 0.17 +/- 0.02 U/g; n = 11). The daily sputum amount significantly decreased from 94.6 +/- 21.6 to 58.1 +/- 17.8 ml (n = 13, p < 0.01) in the GM group, whereas it increased from 78.6 +/- 25.4 ml to 120.5 +/- 33.9 ml (n = 11, p < 0.05) in the saline group. The change in the amount of daily sputum was related to that in the sputum MPO level in the GM group (r = 0.61; p < 0.01). Inhalation of GM, but not saline, significantly (p < 0.05) increased the value of peak expiratory flow (PEF) from 186.4 +/- 25.1 to 216.4 +/- 26.4 L/min and decreased the variability of PEF from 24.6 +/- 5.1 to 6.1 +/- 2.3 %. The nocturnal desaturation and the 6-min walking distances were also significantly improved in the GM group (11.2 +/- 3.8 to 0.6 +/- 0.5 min/h; 324.9 +/- 43.1 to 408.1 +/- 25.9 m; p < 0.05; respectively), but not in the saline group. Subjective improvements in the Borg scale and self-sputum assessment were found in the GM group only. In conclusion, aerosolized GM is effective in improving airway hypersecretion and inflammation in patients with bronchiectasis.
Early postnatal dexamethasone therapy for the prevention of chronic lung disease in preterm infants with respiratory distress syndrome: a multicenter clinical trial.
OBJECTIVES: To study whether early postnatal (<12 hours) dexamethasone therapy reduces the incidence of chronic lung disease in preterm infants with respiratory distress syndrome. MATERIALS AND METHODS: A multicenter randomized, double-blind clinical trial was undertaken on 262 (saline placebo, 130; dexamethasone, 132) preterm infants (<2000 g) who had respiratory distress syndrome and required mechanical ventilation shortly after birth. The sample size was calculated based on the 50% reduction in the incidence of chronic lung disease when early dexamethasone is used, allowing a 5% chance of a type I error and a 10% chance of a type II error. For infants who received dexamethasone, the dosing schedules were: 0.25 mg/kg/dose every 12 hours intravenously on days 1 through 7; 0.12 mg/kg/dose every 12 hours intravenously on days 8 through 14; 0.05 mg/kg/dose every 12 hours intravenously on days 15 through 21; and 0. 02 mg/kg/dose every 12 hours intravenously on days 22 through 28. A standard protocol for respiratory care was followed by the participating hospitals. The protocol emphasized the criteria of initiation and weaning from mechanical ventilation. The diagnosis of chronic lung disease based on oxygen dependence and abnormal chest roentgenogram was made at 28 days of age. To assess the effect of dexamethasone on pulmonary inflammatory response, serial tracheal aspirates were assayed for cell counts, protein, leukotriene B4, and 6-keto prostaglandin F1alpha. All infants were observed for possible side effects, including hypertension, hyperglycemia, sepsis, intraventricular hemorrhage, retinopathy of prematurity, cardiomyopathy, and alterations in calcium homeostasis, protein metabolism, and somatic growth. RESULTS: Infants in the dexamethasone group had a significantly lower incidence of chronic lung disease than infants in the placebo group either judged at 28 postnatal days (21/132 vs 40/130) or at 36 postconceptional weeks (20/132 vs 37/130). More infants in the dexamethasone group than in the placebo group were extubated during the study. There was no difference between the groups in mortality (39/130 vs 44/132); however, a higher proportion of infants in the dexamethasone group died in the late study period, probably attributable to infection or sepsis. There was no difference between the groups in duration of oxygen therapy and hospitalization. Early postnatal use of dexamethasone was associated with a significant decrease in tracheal aspirate cell counts, protein, leukotriene B4, and 6-keto prostaglandin F1alpha, suggesting a suppression of pulmonary inflammatory response. Significantly more infants in the dexamethasone group than in the placebo group had either bacteremia or clinical sepsis (43/132 vs 27/130). Other immediate, but transient, side effects observed in the dexamethasone group are: an increase in blood glucose and blood pressure, cardiac hypertrophy, hyperparathyroidism, and a transient delay in the rate of growth. CONCLUSIONS: In preterm infants with severe respiratory distress syndrome requiring assisted ventilation shortly after birth, early postnatal dexamethasone therapy reduces the incidence of chronic lung disease, probably on the basis of decreasing the pulmonary inflammatory process during the early neonatal period. Infection or sepsis is the major side effect that may affect the immediate outcome. Other observable side effects are transient. In view of the significant side effects and the lack of overall improvement in outcome and mortality, and the lack of long term follow-up data, the routine use of early dexamethasone therapy is not yet recommended.
Hemodynamic studies and esophageal morphometric analyses in portal hypertensive rats with left adrenal vein ligation.
BACKGROUND: Despite many attempts to create esophageal varices in experimental animals, most of them have failed. This study investigated whether rats with partial portal vein ligation (PVL) and left adrenal vein ligation (LAL) develop hyperdynamic circulation and dilated esophageal submucosal veins as compared with sham-operated (Sham) plus LAL rats. METHODS: Two series of experiments were performed to measure (a) systemic and portal hemodynamics and (b) the cross-sectional area of esophageal submucosal veins in Sham, PVL, Sham plus LAL, and PVL plus LAL rats. Hemodynamic studies with a thermodilution technique and esophageal morphometric analyses were performed 14 days after the operation. RESULTS: PVL rats with or without LAL had a significantly lower mean arterial pressure and systemic vascular resistance accompanied by a significantly cardiac index and portal pressure than Sham rats with or without LAL (P < 0.05). LAL did not induce changes in mean arterial pressure, cardiac index, systemic vascular resistance, hear rate, or portal pressure in either Sham or PVL rats (P > 0.05). The mean cross-sectional area of esophageal submucosal veins in PVL rats with LAL (7340 +/- 833 microns2) was significantly larger than that in Sham rats with LAL (4236 +/- 556 microns2; P < 0.05). There was no significant difference in the mean cross-sectional area of esophageal submucosal veins between PVL and Sham rats without LAL. CONCLUSIONS: PVL rats with LAL developed hyperdynamic circulation similar to PVL rats without LAL. In addition, PVL plus LAL rats had larger esophageal submucosal veins than Sham plus LAL rats. This study shows that the esophageal submucosal veins of the 14-day partially portal vein-ligated rats with LAL resemble the structural abnormalities observed in human esophageal varices, suggesting that this model could be useful to investigate this entity.
Hyperdynamic circulation of cirrhotic rats: role of substance P and its relationship to nitric oxide.
BACKGROUND: It has been suggested that excessive formation of nitric oxide (NO) is responsible for the hyperdynamic circulation observed in portal hypertension. Substance P is a neuropeptide partly cleared by the liver and causes vasodilatation through the activation of the endothelial NO pathway. However, there are no previously published data concerning the plasma level of substance P in cirrhotic rats and its relationship to NO. METHODS: Plasma concentrations of substance P and nitrate/nitrite (an index of NO production) were determined in control rats and cirrhotic rats with or without ascites using an enzyme-linked immununosorbent assay and a colorimetric assay, respectively. In addition, systemic and portal hemodynamics were evaluated by a thermodilution technique and catheterization. RESULTS: Cirrhotic rats with and without ascites had a lower systemic vascular resistance (2.6 +/- 0.2 and 3.9 +/- 0.4 mmHg ml(-1) x min x 100 g body weight, respectively) and higher portal pressure (14.6 +/- 0.6 and 11.3 +/- 1.8 mmHg) than control rats (6.5 +/- 0.3 mmHg x ml(-1) x min x 100 g BW and 6.8 +/- 0.2 mmHg, respectively, P < 0.05), and cirrhotic rats with ascites had the lowest systemic vascular resistance. Plasma levels of nitrate/nitrite progressively increased in relation to the severity of liver dysfunction (control rats, 2.7 +/- 0.5 nmol/ml; cirrhotic rats without ascites, 5.6 +/- 1.3 nmol/ml; cirrhotic rats with ascites, 8.3 +/- 2.2 nmol/ml; P < 0.05). Cirrhotic rats with ascites displayed higher plasma values of substance P (57.7 +/- 5.9 pg/ml) than cirrhotic rats without ascites (37.9 +/- 3.1 pg/ml, P < 0.05) and control rats (30.1 +/- 1.0 pg/ml, P < 0.05). There was no significant difference in plasma substance P values between control rats and cirrhotic rats without ascites (P > 0.05). No correlation was found between plasma levels of substance P and nitrate/nitrite (r = 0.318, P > 0.05). CONCLUSIONS: Excessive formation of NO may be responsible, at least partly, for the hemodynamic derangements in cirrhosis. Although substance P may not participate in the initiation of a hyperdynamic circulation in cirrhosis, it may contribute to the maintenance of the hyperdynamic circulation observed in cirrhotic rats with ascites.
Hyperdynamic circulation in prehepatic portal hypertension: role of tumor necrosis factor-alpha.
BACKGROUND: Portal hypertension is associated with a hyperdynamic circulation characterized by increased cardiac output and reduced systemic vascular resistance. Tumor necrosis factor-alpha (TNF-alpha) is a peptide mediator released by mononuclear cells on activation by endotoxin, tissue injury and malignancy. This cytokine induces vasodilatation by activating nitric oxide synthesis. The aim of this study is to investigate if TNF-alpha is involved in the pathogenesis of hyperdynamic circulation observed in portal vein-ligated (PVL) rats. METHODS: Systemic and portal hemodynamics were determined in seven PVL and five sham-operated (SHAM) rats using a thermodilution technique. In addition, plasma TNF-alpha concentrations were determined in another 34 PVL and 16 SHAM rats using commercially available enzyme-linked immunosorbent assay. RESULTS: PVL rats had a significantly lower mean arterial pressure (109 +/- 17 mmHg vs. 133 +/- 12 mmHg, p < 0.001) and systemic vascular resistance (2.5 +/- 0.6 mmHg.ml-1.min.100 g BW vs. 4.6 +/- 0.8 mmHg.ml-1.min.100 g BW, p < 0.001) accompanied by a significantly higher portal pressure (14 +/- 1.9 mmHg vs. 9 +/- 2.1 mmHg, p < 0.001) and cardiac index (47.0 +/- 12.1 ml.min-1.100 g BW-1 vs. 29.3 +/- 3.5 ml.min-1.100 g BW-1, p < 0.001) when compared with SHAM rats. Also, PVL rats had significantly higher plasma levels of TNF-alpha as compared with SHAM rats (13.8 +/- 0.9 pg/ ml vs. 11.1 +/- 0.5 pg/ml, p < 0.05). CONCLUSIONS: This study suggests that elevated plasma levels of TNF-alpha observed in PVL rats may participate in the development and/or maintenance of the hyperdynamic circulation occurring in prehepatic portal hypertension.
Plasma substance P levels in patients with liver cirrhosis: relationship to systemic and portal hemodynamics.
OBJECTIVES: Nitric oxide has been proposed as being responsible for the hyperdynamic circulation observed in portal hypertensive states. Substance P, a neuropeptide partly cleared by liver, induces vasodilation through the activation of the endothelial nitric oxide pathway. This study investigated the plasma levels of substance P in cirrhotic patients and the relationship of these levels to systemic and portal hemodynamics. METHODS: Sixty-four patients with cirrhosis and 53 healthy controls had blood samples taken for determining plasma values of substance P by ELISA. Systemic and portal hemodynamics were measured on the same day of blood sampling using a Swan-Ganz catheterization and thermodilution technique. RESULTS: Plasma levels of substance P were higher in cirrhotic patients than in healthy controls (45.7 +/- 2.0 vs 32.9 +/- 1.0 pg/ml, p < 0.001) and directly correlated with Child-Pugh's score (r = 0.52, p < 0.0001). Compared with compensated cirrhotic patients, decompensated cirrhotic patients had higher plasma levels of substance P accompanied by a lower systemic vascular resistance and higher hepatic venous pressure gradient. There was no significant correlation between plasma levels of substance P and systemic vascular resistance and hepatic venous pressure gradient. In addition, no significant difference in plasma levels of substance P was observed between cirrhotic patients with and cirrhotic patients without a hepatic venous pressure gradient > 12 mm Hg or between patients with and patients without large esophageal varices. CONCLUSIONS: Plasma levels of substance P are increased in patients with cirrhosis and may contribute to the pathogenesis and/or maintenance of hyperdynamic circulation in decompensated patients. The severity of cirrhosis is more important than portal hypertension and the severity of esophageal varices for the development of increased plasma substance P levels.
[The clinical application of forced expiration technique in patients with mucus hypersecretion].
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Sequential changes of esophageal motility after endoscopic injection sclerotherapy or variceal ligation for esophageal variceal bleeding: a scintigraphic study.
OBJECTIVE: Endoscopic injection sclerotherapy and variceal ligation are two popular endoscopic methods used to treat esophageal variceal hemorrhage. These two methods have not been compared with regard to esophageal dysfunction after treatment. This is a prospective investigation of esophageal dysmotility after endoscopic injection sclerotherapy and variceal ligation. METHODS: Sequential changes of esophageal motility after endoscopic injection sclerotherapy (n = 25) and variceal ligation (n = 25) were investigated in 50 cirrhotic patients with recent variceal bleeding. Another 22 cirrhotics without esophageal varices were included as controls. Radionuclide esophageal transit tests were performed before initial endoscopic treatment, and 1 and 3 months after variceal eradication. RESULTS: The baseline esophageal transit time was longer in both the sclerotherapy (n = 25, 7.8 +/- 1.4 s) and ligation groups (n = 25, 8.2 +/- 1.8 s) than in controls (n = 22, 6.7 +/- 0.7 s, p < 0.005). The transit time was longer in patients with large varices than in those with small varices (8.3 +/- 1.7 vs. 7.2 +/- 0.7 s, p < 0.05). In the sclerotherapy group, the transit time was prolonged 1 month after variceal eradication, compared with its pretreatment state (n = 20, 7.6 +/- 1.5 vs. 10.0 +/- 2.2 s, p < 0.0001) but was shortened at 3 months compared with 1 month after variceal eradication (n = 12, 10.7 +/- 1.5 vs. 8.6 +/- 2.2 s, p < 0.05). Multiple regression analysis showed that the number of treatment sessions required to eradicate varices was the only significant factor associated with prolonged transit time (p < 0.05). In the ligation group, the transit time changed little at 1 month or 3 months after variceal eradication. CONCLUSIONS: Impairment of esophageal motility can be significant with endoscopic injection sclerotherapy but is reversible. However, endoscopic variceal ligation exerts no significant impact on esophageal motility.
Regulation of dynamin I GTPase activity by G protein betagamma subunits and phosphatidylinositol 4,5-bisphosphate.
Dynamin I is a 100-kDa GTPase that plays an important role in the recycling of synaptic vesicles. Hydrolysis of GTP by dynamin is thought to be a critical step in fission of coated pits to form coated vesicles. We report that the heterotrimeric G protein betagamma subunit complex (Gbetagamma) and phosphatidylinositol 4, 5-bisphosphate (PtdIns(4,5)P2) are negative and positive regulators of dynamin GTPase activity, respectively. Furthermore, the apparent affinity of dynamin for Gbetagamma is substantially enhanced by PtdIns(4,5)P2. However, the GTPase activity of oligomeric dynamin is unaffected by Gbetagamma. The effects of heterotrimeric G proteins on endocytosis may thus be mediated directly and not involve more remote aspects of their signaling properties.
A population-based epidemiological study of human T-cell leukemia virus type I infection in Kin-Hu, Kinmen.
Kinmen is a group of small islands located between Taiwan and Fu-Kien Province of mainland China. The general population in Kinmen are descendants of immigrants from mainland China who began arriving around 317 A.D. Since it has been reported that 0.48% of adults in Taiwan have HTLV-I infection, the decision was made to conduct a community-based epidemiological study in Kinmen to understand the origin and dissemination of HTLV-I in north-east Asia. Over 68% of residents of Kin-Hu township in Kinmen over 30 years of age participated in this study. Eight of 1,425 males and 14 of 1,595 females had HTLV-I infection. Antibody reactivities were further tested by Western blot assays with HTLV-I or HTLV-II type-specific recombinant envelope glycoproteins, and it was determined that all of those infected had HTLV-I and none had HTLV-II. Logistic regression was used for multivariate analysis. The final model indicated that the significant factors associated with HTLV-I infection in Kinmen were age and coastal residency. Age was positively correlated with HTLV-I infection. The eastern coastal area had a rate of HTLV-I infection 3.1 times higher than other areas in Kin-Hu. Further genetic analysis in Kinmen is needed to elucidate a relationship with other HTLV-I isolates in the world.
Inhibition of HIV-1 replication in viral mutants with altered TAR RNA stem structures.
Human immunodeficiency virus type 1 (HIV-1) Tat-mediated trans-activation requires the structural integrity of TAR RNA and the cooperative interaction of human host cell proteins. The TAR domain, minimally required for tat response, includes the Tat binding pyrimidine bulge, the TAR RNA upper stem, and the loop sequences. However, little is known about the significance of the 5'-stem structure of TAR in the regulation of viral growth. We designed viral mutations, specifically in the TAR RNA lower stem structure, and studied their effects on the kinetics of viral growth in T-lymphocyte cell lines and in activated human peripheral blood mononuclear cells. Mutations that destabilized the lower TAR stem structure inhibited viral growth to various degrees in different CD4+ T-cells. These results suggest that the structural integrity of the lower stem structure of TAR plays an important role in viral growth, presumably by binding to specific host cell proteins that stabilize Tat-TAR interactions.
Overexpression of protein kinase C epsilon is oncogenic in rat colonic epithelial cells.
We have analysed the expression of five protein kinase C [PKC] isoforms in an in vitro model using nontumorigenic rat colonic epithelial cells FRC/TEX CL D [D/WT] and in the related tumorigenic Ha-ras-transformed FRC/TEX CL D/H-ras line [D/ras]. The PKC subspecies alpha, delta, epsilon and xi were expressed at the protein level in both D/WT and D/ras cells, while beta PKC was undetectable in both lines. The levels of expression of the delta and xi isoforms were similar in D/WT and D/ras cells. Alpha PKC expression was decreased and epsilon PKC was increased in D/ras cells compared to the D/WT line. To assess whether overexpression of epsilon PKC was linked to the transformed phenotype, we have generated from D/WT cells two clones (D/epsilon-5 and D/epsilon-9) which stably overexpress epsilon PKC about fivefold. Overexpression of epsilon PKC caused marked morphological changes in both transfected clones, which were accompanied by increased saturation densities and anchorage-independent colony formation in semisolid agar. These growth effects were attenuated or reversed by chronic incubation with phorbol 12-myristate 13-acetate. Furthermore, D/epsilon-5 and D/epsilon-9 cells formed tumors in athymic nude mice with 100% incidence while the parental D/WT or vector alone (D/MV12) controls produced no tumors. We conclude that epsilon PKC can act as an oncoprotein when modestly overproduced in nontumorigenic D/WT colonic cells, and that this isoform of PKC may be linked to ras-modulated signal transduction leading to neoplastic transformation in colonic epithelium.
Comparison of two techniques for castration of llamas.
OBJECTIVE: To compare a prescrotal castration technique with the conventional bilateral scrotal incision technique for castration of llamas. DESIGN: Prospective randomized controlled trial. ANIMALS: 10 clinically normal, sexually intact male llamas. PROCEDURE: Five llamas were castrated by use of a 5-cm skin incision located 2 to 3 cm lateral to the ventral midline and approximately 15 cm cranial to the scrotum, which was closed with absorbable suture material to allow primary healing. Five other llamas were castrated via a more conventional technique, with a 5-cm scrotal incision positioned directly over each testis, which was allowed to heal by second intention. RESULTS: The prescrotal technique required significantly more time to complete; however, no additional anesthesia was required to complete the longer procedure. Llamas castrated with the prescrotal technique required less aftercare and had less incisional pain when the area was palpated. CLINICAL IMPLICATIONS: Both techniques are safe and effective. Some clients, however, find the prescrotal technique more aesthetically acceptable. The prescrotal technique may be more clinically important where fly control is difficult.